Combining canaloplasty with clear corneal phacoemulsification seems to allow further improvement of the aqueous outflow and provides higher IOP reduction than performed separately due to alterations of the architecture of the angle resulting in a more open configuration [ 15- 17].
Indeed, a growing number of permeability inducing factors (PIFs) was shown to elicit signaling mechanisms culminating in VE-cadherin destabilization and global alteration of the junctional architecture.
Moreover, fibrotic septa composed of collagens and α-smooth muscle actin-positive cells were found between the central and portal veins, indicating alteration of the parenchymal architecture.
Early fibrosis associates deposition of collagen in the Disse space with alteration of the sinusoidal architecture, resulting in a decreased portal venous flow, which is counteracted by an increase in hepatic arterial flow (buffer response).
The disruption of homeostatic mechanisms leads to alteration of the original architecture of the vessel and its biological responsiveness, contributing to acute or chronic diseases such as stroke, hypertension, and atherosclerosis.
A common characteristic of organ-specific autoimmune diseases is the mononuclear, mainly lymphocytic infiltration of the target organ, leading to alteration of the normal architecture and loss of function.
In order to test whether the B cell depletion and alteration of the splenic architecture, induced by the treatment, would influence humoral immune responses, mice were immunized with NIP-ficoll or NIP-ovalbumin 10 days after treatment with 9B9 mAb.
If confirmed by future studies, loss of Shank in placozoans would imply disruption or at least considerable alteration of the macromolecular architecture of the PSD-like protein complex.
Idiopathic focal segmental glomerulosclerosis (FSGS) is a clinicopathologic entity characterized by alteration of the molecular architecture of podocytes and slit diaphragms with disruption of the glomerular filtration barrier (GFB) and consequent proteinuria.
The expression and retention of this exogenous mutant protein in resting and proliferating chondrocytes resulted in a chronic cell stress response, growth plate dysplasia and reduced bone growth, without inducing any alterations to the architecture and organization of the cartilage ECM.
